Reduction of Ethanol‐Derived Acetaldehyde Induced Motivational Properties by <scp>l</scp>‐Cysteine

Peana, Alessandra Tiziana; Assaretti, A.; Muggironi, Giulia; Enrico, Paolo; Diana, Marco

doi:10.1111/j.1530-0277.2008.00809.x

Cited by 33 publications

(47 citation statements)

References 40 publications

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“…In Wistar rats, pretreated i.p. with saline or L-cysteine, followed by intragastric administration of saline, ethanol , or ACD, L-cysteine dose-dependently prevented both ethanol and ACD-induced conditioned place preference [248]. In the same animal model, pretreatment with L-cysteine reduced both acquisition and maintenance of oral ethanol self-administration behaviour [249].…”

Section: Acetaldehyde (Acd)mentioning

confidence: 97%

Turning the Clock Ahead: Potential Preclinical and Clinical Neuropharmacological Targets for Alcohol Dependence

Leggio¹,

Cardone²,

Ferrulli³

et al. 2010

curr pharm des

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Treating alcohol use disorders represents a main goal in public health, but the effect of current medications is modest. Thus, in the last few years, research has been focusing on identifying new neuropharmacological targets for alcohol dependence. This review will summarize recent research, which has identified new targets to treat alcohol dependence. A variety of systems have been investigated, such as the endocannabinoid system, modulators of glutamatergic transmission, corticotropin-releasing factor (CRF), neuropeptide Y (NPY), nociceptin, glial cell line-derived neurotrophic factor (GDNF), acetaldehyde (ACD), substance P and Neurokinin 1 (NK1) receptor, nicotinic acetylcholine receptors (nAchRs), alpha-adrenergic receptor, and many others. Compared to preclinical studies, only a few clinical studies have been conducted so far. Thus, there is a critical need to translate successful preclinical results into human clinical trials. However, since some clinical studies have failed to replicate preclinical findings, future research will have not only to identify more efficacious medications, but also delineate the best match between a particular pharmacotherapy with a specific alcoholic subtype.

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Section: Acetaldehyde (Acd)mentioning

confidence: 97%

Turning the Clock Ahead: Potential Preclinical and Clinical Neuropharmacological Targets for Alcohol Dependence

Leggio¹,

Cardone²,

Ferrulli³

et al. 2010

curr pharm des

Self Cite

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show abstract

“…These investigations have been performed, in naïve rodents, after intragastric acetaldehyde or ethanol (passive) administration on CPP as well as on oral (operant) self-administration studies. In CPP experiments the inhibition of ADH1 (Peana et al, 2008) or catalase (Font et al, 2008) as well as the reduction of acetaldehyde bioavailability, by the use of sequestering agents, impairs the acquisition of ethanol-elicited CPP (Peana et al, 2008, 2009; Ledesma et al, 2013). Furthermore, acetaldehyde itself elicits the acquisition of CPP (Spina et al, 2010) through the activation of extracellular signal regulated kinase pathway via a DA D 1 receptor-mediated mechanism (Ibba et al, 2009; Spina et al, 2010; Vinci et al, 2010).…”

Section: Neurobiological Effects Of Ethanol and Role Of Acetaldehydementioning

confidence: 99%

Mystic Acetaldehyde: The Never-Ending Story on Alcoholism

Peana

Sánchez-Catalán

Hipólito

et al. 2017

Front. Behav. Neurosci.

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After decades of uncertainties and drawbacks, the study on the role and significance of acetaldehyde in the effects of ethanol seemed to have found its main paths. Accordingly, the effects of acetaldehyde, after its systemic or central administration and as obtained following ethanol metabolism, looked as they were extensively characterized. However, almost 5 years after this research appeared at its highest momentum, the investigations on this topic have been revitalized on at least three main directions: (1) the role and the behavioral significance of acetaldehyde in different phases of ethanol self-administration and in voluntary ethanol consumption; (2) the distinction, in the central effects of ethanol, between those arising from its non-metabolized fraction and those attributable to ethanol-derived acetaldehyde; and (3) the role of the acetaldehyde-dopamine condensation product, salsolinol. The present review article aims at presenting and discussing prospectively the most recent data accumulated following these three research pathways on this never-ending story in order to offer the most up-to-date synoptic critical view on such still unresolved and exciting topic.

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“…Mice exhibit a decrease in EtOH CPP and a reduction in EtOH-induced motor depression when treated with D-penicillamine (Font et al, 2005, 2006a). L-cysteine has been found to reduce nose-poke responding for ACD and EtOH during acquisition, maintenance, and reinstatement phases of testing (Peana et al, 2010, 2012) as well as inhibit EtOH and ACD induced CPP (Peana et al, 2009). Peripheral and central (intra-VTA) exposure to D-penicillamine significantly reduced expression of the alcohol-deprivation effect (ADE) as observed by a lack on an increase in EtOH consumption during the initial 3 post-abstinence measurements (Orrico et al, 2013).…”

Section: Implication Of Acd In the Central Actions Of Etohmentioning

confidence: 99%

Elucidating the biological basis for the reinforcing actions of alcohol in the mesolimbic dopamine system: the role of active metabolites of alcohol

Deehan¹,

Hauser²,

Wilden³

et al. 2013

Front. Behav. Neurosci.

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The development of successful pharmacotherapeutics for the treatment of alcoholism is predicated upon understanding the biological action of alcohol. A limitation of the alcohol research field has been examining the effects of alcohol only and ignoring the multiple biological active metabolites of alcohol. The concept that alcohol is a “pro-drug” is not new. Alcohol is readily metabolized to acetaldehyde within the brain. Acetaldehyde is a highly reactive compound that forms a number of condensation products, including salsolinol and iso-salsolinol (acetaldehyde and dopamine). Recent experiments have established that numerous metabolites of alcohol have direct CNS action, and could, in part or whole, mediate the reinforcing actions of alcohol within the mesolimbic dopamine system. The mesolimbic dopamine system originates in the ventral tegmental area (VTA) and projects to forebrain regions that include the nucleus accumbens (Acb) and the medial prefrontal cortex (mPFC) and is thought to be the neurocircuitry governing the rewarding properties of drugs of abuse. Within this neurocircuitry there is convincing evidence that; (1) biologically active metabolites of alcohol can directly or indirectly increase the activity of VTA dopamine neurons, (2) alcohol and alcohol metabolites are reinforcing within the mesolimbic dopamine system, (3) inhibiting the alcohol metabolic pathway inhibits the biological consequences of alcohol exposure, (4) alcohol consumption can be reduced by inhibiting/attenuating the alcohol metabolic pathway in the mesolimbic dopamine system, (5) alcohol metabolites can alter neurochemical levels within the mesolimbic dopamine system, and (6) alcohol interacts with alcohol metabolites to enhance the actions of both compounds. The data indicate that there is a positive relationship between alcohol and alcohol metabolites in regulating the biological consequences of consuming alcohol and the potential of alcohol use escalating to alcoholism.

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Reduction of Ethanol‐Derived Acetaldehyde Induced Motivational Properties by l‐Cysteine

Abstract: The present results further underscore the role of EtOH-derived ACD in EtOH-induced motivational properties. l-cysteine, by binding EtOH-derived ACD, would deprive it of its rewarding properties and reduce its abuse liability.

Cited by 33 publications

References 40 publications

Turning the Clock Ahead: Potential Preclinical and Clinical Neuropharmacological Targets for Alcohol Dependence

Turning the Clock Ahead: Potential Preclinical and Clinical Neuropharmacological Targets for Alcohol Dependence

Mystic Acetaldehyde: The Never-Ending Story on Alcoholism

Elucidating the biological basis for the reinforcing actions of alcohol in the mesolimbic dopamine system: the role of active metabolites of alcohol

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